The mechanism for regulating the critical temperature (TC) of metal-insulator transition (MIT) in ions-doped VO2 systems is still a matter of debate, in particular, the unclear roles of lattice distortion and charge doping effects. To rule out the charge doping effect on the regulation of TC, we investigated Ti4+-doped VO2 (TixV1-xO2) system. It was observed that the TC of TixV1-xO2 samples first slightly decreased and then increased with increasing Ti concentration. X-ray absorption fine structure (XAFS) spectroscopy was used to explore the electronic states and local lattice structures around both Ti and V atoms in TixV1-xO2 samples. Our results revealed the local structure evolution from the initial anatase to the rutile-like structure around the Ti dopants. Furthermore, the host monoclinic VO2 lattice, specifically, the VO6 octahedra would be subtly distorted by Ti doping. The distortion of VO6 octahedra and the variation of TC showed almost the similar trend, confirming the direct effect of local structural perturbations on the phase transition behavior. By comparing other ion-doping systems, we point out that the charge doping is more effective than the lattice distortion in modulating the MIT behavior of VO2 materials.

Metabolic disease subclinical hypothyroidism (SCH) is closely associated with depression-like behavior both in human and animal studies, and our previous studies have identified the antidepressant effect of resveratrol (RES) in stressed rat model. The aim of this study was to investigate whether RES would manifest an antidepressant effect in SCH rat model and explore the possible mechanism. A SCH rat model was induced by hemi-thyroid electrocauterization, after which the model rats in the RES and LT4 groups received a daily intragastric injection of RES at the dose of 15 mg/kg or LT4 at the dose of 60 μg/kg for 16 days. The rats’ plasma concentrations of thyroid hormones were measured. Behavioral performance and hypothalamic–pituitary–adrenal (HPA) activity were evaluated. The protein expression levels of the Wnt/β-catenin in the hippocampus were detected by western blot. The results showed that RES treatment downregulated the elevated plasma thyroid-stimulating hormone concentration and the hypothalamic mRNA expression of thyrotropin-releasing hormone in the SCH rats. RES-treated rats showed increased rearing frequency and distance in the open-field test, increased sucrose preference in the sucrose preference test, and decreased immobility in the forced swimming test compared with SCH rats. The ratio of the adrenal gland weight to body weight, the plasma corticosterone levels, and the hypothalamic corticotrophin-releasing hormone mRNA expression were reduced in the RES-treated rats. Moreover, RES treatment upregulated the relative ratio of phosphorylated-GSK3β (p-GSK3β)/GSK3β and protein levels of p-GSK3β, cyclin D1, and c-myc, while downregulating the relative ratio of phosphorylated-β-catenin (p-β-catenin)/β-catenin and expression of GSK3β in the hippocampus. These findings suggest that RES exerts anxiolytic- and antidepressant-like effect in SCH rats by downregulating hyperactivity of the HPA axis and regulating both the HPT axis and the Wnt/β-catenin pathway.

The acute-phase proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) demonstrate high-level expression and pleiotropic biological effects, and contribute to the progression and persistence of rheumatoid arthritis (RA). Acid hydrarthrosis is also an important pathological characteristic of RA, and the acid-sensing ion channel 1a (ASIC1a) plays a critical role in acidosis-induced chondrocyte cytotoxicity. However, the roles of IL-1β and TNF-α in acid-induced apoptosis of chondrocytes remain unclear. Rat adjuvant arthritis and primary articular chondrocytes were used as in vivo and in vitro model systems, respectively. ASIC1a expression in articular cartilage was increased and highly colocalized with nuclear factor (NF)-κB expression in vivo. IL-1β and TNF-α could upregulate ASIC1a expression. These cytokines activated mitogen-activated protein kinase and NF-κB pathways in chondrocytes, while the respective inhibitors of these signaling pathways could partially reverse the ASIC1a upregulation induced by IL-1β and TNF-α. Dual luciferase and gel-shift assays and chromatin immunoprecipitation-polymerase chain reaction demonstrated that IL-1β and TNF-α enhanced ASIC1a promoter activity in chondrocytes by increasing NF-κB DNA-binding activities, which was in turn prevented by the NF-κB inhibitor ammonium pyrrolidinedithiocarbamate. IL-1β and TNF-α also decreased cell viability but enhanced LDH release, intracellular Ca concentration elevation, loss of mitochondrial membrane potential, cleaved PARP and cleaved caspase-3/9 expression, and apoptosis in acid-stimulated chondrocytes, which effects could be abrogated by the specific ASIC1a inhibitor psalmotoxin-1 (PcTX-1), ASIC1a-short hairpin RNA or calcium chelating agent BAPTA-AM. These results indicate that IL-1β and TNF-α can augment acidosis-induced cytotoxicity through NF-κB-dependent up-regulation of ASIC1a channel expression in primary articular chondrocytes.

Extracellular vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, play an important role in cellular communication during skeletal growth and homeostasis. Bioactive molecules carried by EVs are transported to neighboring and distant cells to trigger a series of signaling cascades influencing bone homeostasis. The bioactive activities of osteoclast-derived EVs include regulation of osteoclastogenesis and osteoclast–osteoblast communication. As osteoclast-derived EVs have the potential to regulate osteoclasts and osteoblasts, their application in osteoporosis and other bone metabolic disorders is currently under investigation. However, very few reviews of osteoclast-derived EVs in bone remodeling regulation have yet been published. This article aims to review recent advances in this field, summarizing a new regulator of osteoclastogenesis and osteoclast–osteoblast communication mediated by osteoclast-derived EVs. We will analyze the major challenges in the field and potential for the therapeutic application of EVs.

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The mechanism for the decreasing critical temperature (T(C)) of the metal-insulator transition (MIT) in vanadium dioxide (VO2) by tungsten (W) doping is a matter of debate. Here, to clarify the correlation between W doping and T(C), the electronic and geometrical structures around W and V atoms in W(x)V(1-x)O2 samples are systematically investigated by X-ray absorption fine structure (XAFS) spectroscopy. The evidence of electron doping of W(6+) ions in VO2 is obtained from the reduction of V(4+) to V(3+) ions. This kind of electron doping has been considered to favor the MIT process. Moreover, from the XAFS results, the local rutile structure around W dopants is identified even at low doping, and acts as the structure-guided domain to facilitate the MIT in VO2. Considering the electronic band structures of W(x)V(1-x)O2 samples, the internal stresses induced by W(6+) doping yield the detwisting of the nearby monoclinic VO2 lattice. This lattice detwisting will drive the downward shift of the π* electron band and a smaller separation between antibonding and bonding d∥ orbitals in the band structure of VO2, which induces the decreased band gaps of W(x)V(1-x)O2 samples. As a consequence, the potential energy barrier for phase transition is lowered and the reduced T(C) is observed.

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These findings represent some experimental evidence of a potential role for ASICs in the pathogenesis of articular cartilage destruction in rheumatoid arthritis.